Ophthalmology Research
Biochemistry Research
The ophthalmic biochemistry lab has been opened to all clinical faculties in our department and friends outside who brought in a clinical problem for biochemical solution. The major current projects are summarized in the following:
Inflammation and mediators in the alkali-injured eyes: Exposure of the corneal epithelium to alkali produces a small chemotactic factor (CF) to induce PMN infiltration and a Respiratory Burst Factor (RBF) inciting PMN to release its proteolytic enzymes resulting in corneal ulceration. One of the current effort in this laboratory is to identify the chemical structure of CF and RBF in order to design the medication for the treatment of alkali burn. We have already identified CF as a tri-peptide "Proline-Glycine-Proline". The RBF has been identified as a polyunsaturated fatty acid. Additional effort is needed to identify the specific chemical structure of fatty acid with RBF activity. The lipid nature of RBF explains the difficulty to remove RBF by currently available aqueous solvents. It is well known that albumin has a high capacity to bind fatty acids. Therefore, addition of albumin to saline should be effective to remove fatty acids released from damaged epithelial cells.
Free radical and degenerative eye diseases: Light induced free radical is toxic to eye tissues. Our effort is directed to study the physiological mechanism by which the retina is protected from free radical damage. This study includes 2 parts.
Clearance of free radical by ascorbate-melanin: After absorbing the light energy, the activated melanin induces ascorbic acid oxidation. Current effort is directed to the detailed chemical mechanism of this light dependent reaction, recycling and mobilization of ascorbic acid in and out of the cells.
Protection of retinal lipids from light damage: The previous study led to a conclusion that ascorbate is the physiological reducing agent for the peroxidase activity of all hemoproteins to prevent H202 accumulation in the aqueous cytoplasm of RPE. However, there is negligible ascorbate-peroxidase in the retina. The high amount of polyunsaturated fatty acids in the retina calls for a study on the reducing agent and the peroxidase which remove lipid hydroperoxide in the hydrophobic biomembranes in the retina. Others have postulated the occurrence of phospholipid hydroperoxide glutathione peroxidase (PHGPX) to protect lipids in biomembranes of heart, testis, liver and brain. Normal tissues should have sufficient vitamin E for PHGPX to operate at maximal rate. Thus, the potency of vitamin E is limited by the concentration of endogenous PHGPX.
Our present effort is directed to purify a large amount of PHGPX from the retina and identify its chemical structure. The knowledge of the chemical structure will allow us to plan an in depth investigation on the metabolism of PHGPX, and to elucidate a way to reinforce the antioxidant capability of the retina by increasing retinal PHGPX activity.
Biochemical mechanism of Glaucoma: Studies on the biochemical changes in aqueous humor of glaucomatous eyes led to the following hypothesis: (1) reduced ascorbate-increased urate is an indicator of free radical damages inside the eye. Increased urate reflects activation of xanthine oxidase to produce excessive free radicals and the occurrence of free radical is indicated from the loss of ascorbate. (2) Fibrin clot could be the major factor of transient glaucoma after eye surgery. Continuous effort is directed to delineate the biochemical factors involved in obstruction of aqueous humor drainage among the wide varieties of glaucoma eyes.
Developmental biology of the eye: Experimental design is directed to ascorbate transport into the optic vesicle during the early development of the eye and the role of ascorbate in the biosynthetic activities and expansion of the eye cup.
Contact Person: Randolph Glickman, Ph.D.
UTHSCSA Department of Ophthalmology, MC-6230
7703 Floyd Curl Drive
San Antonio, TX 78229-3900
(210) 567-8434 voice
(210) 567-8413 FAX
Email:glickman@uthscsa.edu
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© 1996-2005 UTHSCSA Department of Ophthalmology
Updated 07 March 2005